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The traveling-salesman problem can be regarded as an NP-hard problem. To better solve the best solution, many heuristic algorithms, such as simulated annealing, ant-colony optimization, tabu search, and genetic algorithm, were used. However, these algorithms either are easy to fall into local optimization or have low or poor convergence performance. This paper proposes a new algorithm based on simulated annealing and gene-expression programming to better solve the problem. In the algorithm, we use simulated annealing to increase the diversity of the Gene Expression Programming (GEP) population and improve the ability of global search. The comparative experiments results, using six benchmark instances, show that the proposed algorithm outperforms other well-known heuristic algorithms in terms of the best solution, the worst solution, the running time of the algorithm, the rate of difference between the best solution and the known optimal solution, and the convergent speed of algorithms.

Flavonoids have been reported to exhibit prooxidant cytotoxicity against cancer cells, but the underlying mechanism is still poorly understood. Here we investigated the potential mechanism that p53-inducible gene 3 (PIG3), a NADPH:quinone oxidoreductase, mediated the prooxidant cytotoxicity of flavonoids on human hepatoma HepG2 cells. The results showed that flavonoids (apigenin, luteolin, kaempferol, and quercetin) inhibited the growth of HepG2 cells in a dosage- and time-dependent manner, and induced the morphological changes characteristic of apoptosis in HepG2 cells. We also found that expression of PIG3 was increased markedly in HepG2 cells treated with flavonoids at both mRNA and protein levels, which was accompanied by increased intracellular ROS production and a decreased mitochondrial membrane potential (ΔΨm). All these effects were largely reversed through knockdown of the PIG3 gene in HepG2 cells. Western blotting indicated that flavonoids increased cytochrome c release, upregulated the ratio of Bax/Bcl-2, and activated the caspases-9 and -3. Moreover, knockdown of PIG3 could reverse the changes of these apoptotic-related proteins. These results suggest that PIG3 plays an important role in regulating the prooxidant activity and apoptosis-inducing action of flavonoids on HepG2 cells though the ROS-triggered mitochondrial apoptotic pathway.

This updated meta-analysis was performed to clarify the relationship between phytoestrogens and prostate cancer risk. Twenty one case-control and two cohort studies were finally selected for this meta-analysis, totaling 11,346 cases and 140,177 controls. Analytical results showed that daidzein (OR = 0.85; 95% CI: 0.75-0.96), genistein (OR = 0.87; 95% CI: 0.78-0.98), and glycitein (OR = 0.89; 95% CI: 0.81-0.98) were associated with a reduction of prostate cancer risk, but total isoflavones (OR = 0.93; 95% CI: 0.84-1.04), equol (OR = 0.86; 95% CI: 0.66-1.14), total lignans (OROgna.05; 95% CI: 0.54-2.04), secoisolariciresinol (OR = 1.02; 95% CI: 0.83-1.24), matairesinol (OR = 0.91; 95% CI: 0.75-1.11), enterolactone (OR = 0.94; 95% CI: 0.73-1.20), and coumestrol (OR = 0.89; 95% CI: 0.76-1.06) were not. Sensitivity and publication bias analyses demonstrated that the pooled estimates were stable and reliable. The results support the notion that some phytoestrogens may have a role in decreasing the risk of prostate cancer. Additional large and well-designed cohort studies are needed to confirm these relationships.

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We aim to explore the associations between dietary zinc intake and hyperuricemia (HU) in United States (US) adults. 24,975 US adults aged 20 years or older from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2014 were stratified into quintiles based on zinc intake. All dietary intake measured through 24-h dietary recalls. Multivariable logistic regression analysis was performed to examine the association between zinc intake and HU after adjustment for possible confounders. For males, compared with respondents consuming less than 7.33 mg zinc daily, the adjusted odds ratios (ORs) were 0.83 (95% CI, 0.71, 0.97) among those consuming 10.26–13.54 mg zinc daily, 0.78 (95% CI, 0.63–0.96) among those consuming 18.50 mg or greater, and p for the trend was 0.0134. For females, compared with respondents consuming less than 5.38 mg zinc daily, the OR was 0.78 (95% CI, 0.63, 0.97) among those consuming 9.64–12.93 mg zinc daily, and p for the trend was 0.3024. Our findings indicated that dietary zinc intake is inversely associated with HU in US men and women, independent of some major confounding factors.

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PurposeTo investigate the mechanism of the anti-epileptic effect of Ganoderma lucidum polysaccharides (GLP), the changes of intracellular calcium and CaMK II α expression in a model of epileptic neurons were investigated.MethodPrimary hippocampal neurons were divided into: 1) Control group, neurons were cultured with Neurobasal medium, for 3 hours; 2) Model group I: neurons were incubated with Mg2+ free medium for 3 hours; 3) Model group II: neurons were incubated with Mg2+ free medium for 3 hours then cultured with the normal medium for a further 3 hours; 4) GLP group I: neurons were incubated with Mg2+ free medium containing GLP (0.375 mg/ml) for 3 hours; 5) GLP group II: neurons were incubated with Mg2+ free medium for 3 hours then cultured with a normal culture medium containing GLP for a further 3 hours. The CaMK II α protein expression was assessed by Western-blot. Ca2+ turnover in neurons was assessed using Fluo-3/AM which was added into the replacement medium and Ca2+ turnover was observed under a laser scanning confocal microscope.ResultsThe CaMK II α expression in the model groups was less than in the control groups, however, in the GLP groups, it was higher than that observed in the model group. Ca2 + fluorescence intensity in GLP group I was significantly lower than that in model group I after 30 seconds, while in GLP group II, it was reduced significantly compared to model group II after 5 minutes.ConclusionGLP may inhibit calcium overload and promote CaMK II α expression to protect epileptic neurons.